Kidney-urinary tract stone disease (urolithiasis) is a major health problem throughout the world. Most of the stones associated with urolithiasis are composed of calcium oxalate alone or calcium oxalate plus calcium phosphate. Other disease states have also been associated with excess oxalate. These include, vulvodynia, oxalosis associated with end-stage renal disease and with Crohn's disease, and other enteric disease states.
Oxalic acid (and/or its salt-oxalate) is found in a wide diversity of foods, and is therefore, a component of many constituents in human diets. Increased oxalate absorption may occur after foods containing elevated amounts of oxalic acid are eaten. Foods such as spinach and rhubarb are well known to contain high amounts of oxalate, but a multitude of other foods and beverages also contain oxalate. Because oxalate is found in such a wide variety of foods, diets that are low in oxalate and which are also palatable are hard to formulate.
Oxalate is also produced metabolically by normal tissue enzymes. Oxalate (dietary oxalate that is absorbed as well as oxalate that is produced metabolically) is not further metabolized by tissue enzymes and must therefore be excreted. This excretion occurs mainly via the kidneys. The concentration of oxalate in kidney fluids is critical, with increased oxalate concentrations causing increased risk for the formation of calcium oxalate crystals and thus the subsequent formation of kidney stones.
The risk for formation of kidney stones revolves around a number of factors that are not yet completely understood. Kidney-urinary tract stone disease occurs in about 2% of the population in Western countries and about 70% of these stones are composed of calcium oxalate or of calcium oxalate plus calcium phosphate. Some individuals (e.g., patients with intestinal disease such as Crohn's disease, inflammatory bowel disease, or steatorrhea and also patients that have undergone jejunoileal bypass surgery) absorb more of the oxalate in their diets than do others. For these individuals, the incidence of oxalate urolithiasis increases markedly. The increased disease incidence is due to increased levels of oxalate in kidneys and urine, and this, the most common hyperoxaluric syndrome in man, is known as enteric hyperoxaluria. Oxalate is also a problem in patients with end-stage renal disease and there is recent evidence (Solomons et al. [1991] "Calcium citrate for vulvar vestibulitis" Journal of Reproductive Medicine 36:879-882) that elevated urinary oxalate is also involved in vulvar vestibulitis (vulvodynia).
Bacteria that degrade oxalate have been isolated from human feces (Allison et al. [1986] "Oxalate degradation by gastrointestinal bacteria from humans" J. Nutr. 116:455-460). These bacteria were found to be similar to oxalate-degrading bacteria that had been isolated from the intestinal contents of a number of species of animals (Dawson et al. [1980] "Isolation and some characteristics of anaerobic oxalate-degrading bacteria the rumen" Appl. Environ. Microbiol. 40:833-839;Allison and Cook [1981] "Oxalate degradation by microbes of the large bowel of herbivores: the effect of dietary oxalate" Science 212:675-676; Daniel et al. [1987] "Microbial degradation of oxalate in the gastrointestinal tracts of rats" Appl. Environ. Microbiol. 53:1793-1797). These bacteria are different from any previously described organism and have been given both a new species and a new genus name, formigenes (Allison et al. [1985] "Oxalabacter formigenes gen. nov., sp. nov.: oxalate-degrading anaerobes that inhabit the gastrointestinal tract" Arch. Microbiol. 141:1-7).
Not all humans carry populations of O. formigenes in their intestinal tracts (Allison et al. [1995] "Oxalate-degrading bacteria"In Khan, S. R. (ed.), Calcium Oxalate in Biological Systems CRC Press; Doane et al. [1989] "Microbial oxalate degradation: effects on oxalate and calcium balance in humans" Nutrition Research 9:957-964). There are very low concentrations or a complete lack of oxalate degrading bacteria in the fecal samples of persons who have had jejunoileal bypass surgery (Allison et al. [1986] "Oxalate degradation by gastrointestinal bacteria from humans" J. Nutr. 116:455-460).